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Updated: Jul 10, 2026

Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues
08:47

Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues

Published on: May 8, 2016

Heterogeneity of EAE mediated by multiple distinct T-effector subsets

Sara Abromson-Leeman1, Daniel S Ladell, Roderick T Bronson

  • 1Department of Pathology, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA. sara_abromson-leeman@hms.harvard.edu

Journal of Neuroimmunology
|November 3, 2007
PubMed

Both T(H)1 and T(H)17 lymphocytes are implicated in inducing EAE. In mice lacking IFNgamma, T(H)17 are assumed to be the subset responsible for inflammation induction. Here, we demonstrate that IFNgamma KO mice have two additional effector subsets, one that up-regulates T(H)17-associated pro-inflammatory genes, but does not make IL-17 protein, and a second that utilizes IL-12-related elements of the T(H)1 pathway in an IFNgamma-independent manner. In vivo, these two subsets induce demonstrably different disease. By using homogeneous T cell lines, we can dissect the population of autoimmune effector cells, and demonstrate the multiplicity of pro-inflammatory pathways important in disease processes.

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